Islet amyloid polypeptide (amylin)-deficient mice develop a more severe form of alloxan-induced diabetes.

Mulder, H; Gebre-Medhin, S; Betsholtz, C; Sundler, F; Ahrén, B

Mulder, H; Gebre-Medhin, S; Betsholtz, C; Sundler, F; Ahrén, B.

Affiliation

Mulder H; Section for Molecular Signaling, Department of Cell and Molecular Biology, Lund University, SE-221 00 Lund, Sweden. mulder@utsw.swmed.edu

Am J Physiol Endocrinol Metab ; 278(4): E684-91, 2000 Apr.

Article in En | MEDLINE | ID: mdl-10751203

Subject(s)

Amyloid/deficiency; Diabetes Mellitus, Experimental/genetics; Diabetes Mellitus, Experimental/pathology; Animals; Blood Glucose/metabolism; Body Weight/drug effects; Gene Expression/genetics; Gene Expression/physiology; Glucose Tolerance Test; Glucose Transporter Type 2; Immunohistochemistry; In Situ Hybridization; Insulin/biosynthesis; Insulin/blood; Insulin/genetics; Islet Amyloid Polypeptide; Islets of Langerhans/pathology; Male; Mice; Mice, Knockout; Monosaccharide Transport Proteins/metabolism; RNA, Messenger/biosynthesis; RNA, Messenger/genetics; Receptors, Islet Amyloid Polypeptide; Receptors, Peptide/metabolism

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Collection: 01-internacional Database: MEDLINE Main subject: Diabetes Mellitus, Experimental / Amyloid Limits: Animals Language: En Journal: Am J Physiol Endocrinol Metab Journal subject: ENDOCRINOLOGIA / FISIOLOGIA / METABOLISMO Year: 2000 Type: Article Affiliation country: Sweden

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